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Different subcellular populations of L-type Ca2+ channels exhibit unique regulation and functional roles in cardiomyocytes

Journal of molecular and cellular cardiology, 2012-02, Vol.52 (2), p.376-387

2012

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Small GTPase Rab11b regulates degradation of surface membrane L-type Cav1.2 channels

American Journal of Physiology: Cell Physiology, 2011-05, Vol.300 (5), p.C1023-C1033

2011

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Small GTPase Determinants for the Golgi Processing and Plasmalemmal Expression of Human Ether-a-go-go Related (hERG) K+ Channels

The Journal of biological chemistry, 2009-01, Vol.284 (5), p.2844-2853

2009

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Long QT syndrome caveolin-3 mutations differentially modulate K v 4 and Ca v 1.2 channels to contribute to action potential prolongation

The Journal of physiology, 2019-03, Vol.597 (6), p.1531-1551

2019

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Caveolin-3 and Caveolae regulate ventricular repolarization

Journal of molecular and cellular cardiology, 2023-04, Vol.177, p.38-49

2023

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Exome sequencing and systems biology converge to identify novel mutations in the L-type calcium channel, CACNA1C, linked to autosomal dominant long QT syndrome

Circulation. Cardiovascular genetics, 2013-06, Vol.6 (3), p.279

2013

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Long QT syndrome caveolin‐3 mutations differentially modulate Kv4 and Cav1.2 channels to contribute to action potential prolongation

The Journal of physiology, 2019-03, Vol.597 (6), p.1531-1551

2019

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A sympathetic model of L-type Ca2+ channel-triggered arrhythmias

American journal of physiology. Heart and circulatory physiology, 2010-01, Vol.298 (1), p.H3-H4

2010

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A sympathetic model of L-type Ca 2+ channel-triggered arrhythmias

American journal of physiology. Heart and circulatory physiology, 2010-01, Vol.298 (1), p.H3-H4

2010

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Loss of Caveolin-3 Results in QtC Prolongation and Causes Delayed Cardiac Repolarization in a Cardiac-Specific Conditional CAV-3 Knockout Mouse Model

Biophysical journal, 2013-01, Vol.104 (2), p.209a-209a

2013

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Long QT Syndrome-Associated F97C and S141R CaV-3 Mutations Exert Pleiotropic Effects on Cardiac L-Type Calcium Channels

Biophysical journal, 2012-01, Vol.102 (3), p.127a-127a

2012

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Long QT syndrome caveolin-3 mutations differentially modulate Kv 4 and Cav 1.2 channels to contribute to action potential prolongation

The Journal of physiology, 2019-03, Vol.597 (6), p.1531-1551

2019

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Cavβ2 Subunit Associates with Caveolin-3 and Regulates Trafficking and β2adrenergic Receptor Regulation of the Caveolar L-Type Ca2+ Channels

Biophysical journal, 2010-01, Vol.98 (3), p.15a-15a

2010

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Small GTPase Rab11b regulates degradation of surface membrane L-type Ca^sub v^1.2 channels

American Journal of Physiology: Cell Physiology, 2011-05, Vol.300 (5), p.C1023

2011

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Rab11b GTPase Is Expressed In Ventricular Myocardium And Regulates Trafficking Of L-type Ca2+ Channels

Biophysical journal, 2009-02, Vol.96 (3), p.186a-186a

2009

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Abstract 1070: An Unconventional Vesicular Transport Pathway Regulates the Cell Surface Expression of hERG K + Channels

Circulation (New York, N.Y.), 2007-10, Vol.116 (suppl_16)

2007

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Regulation of sarcolemmal turnover of cardiac Ca(v)1.2 L-type calcium channels by the small GTPase Rab11B

Best, Jabe M

2011

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ProQuest

Abstract 19749: Cardiac-specific Deletion of Caveolin-3 Delays Repolarization and Increases Susceptibility to Ventricular Arrhythmia

Circulation (New York, N.Y.), 2015-11, Vol.132 (Suppl_3 Suppl 3), p.A19749-A19749

2015

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Non-communicable chronic diseases, a global public health priority recognized by the United Nations

La Presse médicale (1983), 2011-09, Vol.40 (9 Pt 1), p.787-789

Bousquet, J

2011

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Different subcellular populations of L-type Ca2+ channels exhibit unique regulation and functional roles in cardiomyocytes

Small GTPase Rab11b regulates degradation of surface membrane L-type Cav1.2 channels

Small GTPase Determinants for the Golgi Processing and Plasmalemmal Expression of Human Ether-a-go-go Related (hERG) K+ Channels

Long QT syndrome caveolin-3 mutations differentially modulate K v 4 and Ca v 1.2 channels to contribute to action potential prolongation

Caveolin-3 and Caveolae regulate ventricular repolarization

Exome sequencing and systems biology converge to identify novel mutations in the L-type calcium channel, CACNA1C, linked to autosomal dominant long QT syndrome

Long QT syndrome caveolin‐3 mutations differentially modulate Kv4 and Cav1.2 channels to contribute to action potential prolongation

A sympathetic model of L-type Ca2+ channel-triggered arrhythmias

A sympathetic model of L-type Ca 2+ channel-triggered arrhythmias

Loss of Caveolin-3 Results in QtC Prolongation and Causes Delayed Cardiac Repolarization in a Cardiac-Specific Conditional CAV-3 Knockout Mouse Model

Long QT Syndrome-Associated F97C and S141R CaV-3 Mutations Exert Pleiotropic Effects on Cardiac L-Type Calcium Channels

Long QT syndrome caveolin-3 mutations differentially modulate Kv 4 and Cav 1.2 channels to contribute to action potential prolongation

Cavβ2 Subunit Associates with Caveolin-3 and Regulates Trafficking and β2adrenergic Receptor Regulation of the Caveolar L-Type Ca2+ Channels

Small GTPase Rab11b regulates degradation of surface membrane L-type Ca^sub v^1.2 channels

Rab11b GTPase Is Expressed In Ventricular Myocardium And Regulates Trafficking Of L-type Ca2+ Channels

Abstract 1070: An Unconventional Vesicular Transport Pathway Regulates the Cell Surface Expression of hERG K + Channels

Regulation of sarcolemmal turnover of cardiac Ca(v)1.2 L-type calcium channels by the small GTPase Rab11B

Abstract 19749: Cardiac-specific Deletion of Caveolin-3 Delays Repolarization and Increases Susceptibility to Ventricular Arrhythmia

Non-communicable chronic diseases, a global public health priority recognized by the United Nations

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